Evidence map›Paper›PMID 22507397›Full record

ArticleCell transplantation2012

Low temperature condition prevents hypoxia-induced islet cell damage and HMGB1 release in a mouse model.

Takeshi Itoh, Koji Sugimoto, Morihito Takita, Masayuki Shimoda, Daisuke Chujo, Jeff A SoRelle, Bashoo Naziruddin, Marlon F Levy, Shinichi Matsumoto

Open access · bronzeAbstract read
In one paragraph

Article in Cell transplantation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. HMGB1 in health and disease.Molecular aspects of medicine · 2014
    Review
  10. Optimal method for short-term or long-term islet preservation: comparison of islet culture, cold preservation and cryopreservation.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2014
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Takeshi ItohBaylor Research Institute, Dallas, TX, USA.
Koji Sugimoto
Morihito Takita
Masayuki Shimoda
Daisuke Chujo
Jeff A SoRelle
Bashoo Naziruddin
Marlon F Levy
Shinichi Matsumoto
Baylor University · USBaylor University Medical Center · USCHRISTUS Transplant Institute · US

Funding

Randomized Comparison of Ductal Preservation Solutions for Improving QuantityR21DK090513 · NIDDK · BAYLOR RESEARCH INSTITUTE · PI LEVY, MARLON FRANTZ · 2011 to 2012
$431k
NIDDK NIH HHS 1R21DK090513-019NIDDK NIH HHS R21 DK090513
6 · The paper itself

Abstract

One of the major issues in clinical islet transplantation is the poor efficacy of islet isolation. During pancreas preservation and islet isolation, islets suffer from hypoxia as islets are highly sensitive to hypoxic conditions.Cold preservation has been applied to minimize hypoxia-induced cell damage during organ preservation.However, the studies related to hypoxia-induced islet cell damage during islet isolation are limited. Recently,we demonstrated that mouse islets contain high levels of high-mobility group box 1 protein (HMGB1), and during proinflammatory cytokine-induced damage, islets release HMGB1 outside the cell. The released HMGB1 is involved in the initial events of early islet loss. In the present study, we hypothesize that low temperature conditions could prevent both hypoxia induced islet cell damage and HMGB1 release from islets in a mouse model. Isolated mouse islets underwent normoxic condition (95% air and 5% CO(2)) at 37°C or hypoxic conditions (1% O(2), 5% CO(2), and 94% N(2)) at 37°C (hypoxia-37°C islets), 22°C (hypoxia-22°C islets), or 4°C (hypoxia-4°C islets) for 12 h. In vitro and in vivo viability and functionality tests were performed. HMGB1, IL-6, G-CSF, KC, RANTES, MCP-1, and MIP-1α levels in the medium were measured. Low temperature conditions substantially reduced hypoxia-induced necrosis (p < 0.05) and apoptosis (p < 0.05). In addition, low temperature islet culture significantly increased the insulin secretion from islets by high glucose stimulation (p < 0.05). All of the recipient mice reversed diabetes after receiving the hypoxia-4°C islets but not after receipt of hypoxia-37°C or 22°C islets. The amounts of released HMGB1, IL-6, G-CSF, KC, RANTES, MCP-1, and MIP-1α were significantly reduced in the hypoxia-4°C islets compared to those of the hypoxia-37°C islets (p < 0.05). In conclusion, low temperature conditions could prevent hypoxia-induced islet cell damage, inflammatory reactions in islets, and HMGB1 release and expression. Low temperature conditions should improve the efficacy of isolated islets.

Indexed as

Cell HypoxiaCold TemperatureAnimalsCell SeparationChemokinesCytokinesDiabetes Mellitus, ExperimentalDisease Models, AnimalHMGB1 ProteinInsulinInsulin SecretionIslets of LangerhansIslets of Langerhans TransplantationMaleMiceMice, Inbred C57BLChemokinesCytokinesHMGB1 ProteinInsulin

Identifiers

PMID22507397
PMCPMC4090700
OpenAlexW2013327244

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.